Neuropathology 1, basic principles & Cerebrovascular disease

the 31 pairs of spinal nerves and 12 cranial nerves

Dura tough, fibrous, bridges crevices, attached to skull Arachnoid delicate sealed bag for CSF, bridges crevices Arachnoid trabeculae ropes across subarachnoid space pia mater delicate and dips into crevices

Neurones Glial cells Blood vessels Microglia Connective tissue (meninges)

supporting system for neurones and their dendritic and axonal processes astrocytes (regulate transmission of electrical impulses) oligodendrocytes (wrap around axons forming myelin sheath) ependyma (line the ventricular system)

acute neuronal injury simple neuronal atrophy (in hypoxia) Sub-cellular alterations Axonal reaction

-activation of glutamate receptors and uncontrolled Ca entry into cell they can’t use anaerobic glycolysis

-a reaction within the cell body that is associated with axonal injury -inc RNA and protein synthesis swelling of cell body peripheral displacement of nucleus enlargement of nucleolus central chromatolysis anterograde degeneration of axon occurs distal to sire of injury breakdown of myelin sheath

• a nonspecific reactive change of glial cells in response to damage to the central nervous system • CNS injury • undergo hyperplasia and hypertrophy -N: enlarges, becomes vesicular and nucleolus prominent C: expansion with extension of ramifying processes -nuclei become small and dark and lie in a dense net of processes

• wrap around axons of neurones to from myelin sheath • limiters reaction • demyelinating disorders

• line the ventricular system • limited • local proliferation of sub-ependymal astrocytes to produce small irregularities on the ventricular surfaces termed ependymal granulations • infectious agents e.g. viruses

-fixed macrophage system -proliferating developing elongated nuclei (rod cells) forming aggregates around small foci of tissue necrosis (microglial nodules) Congregate around portions of dying neurones (neuronophagia)

• 15% of CO and 20%of O2 consumed by body • brain requires active aerobic metabolism of glucose -autoregulatory mechanisms (vasculature constricts on response to abnormally high pressure and dilates in response to hypotension) -internal carotid and vertebral arteries = circle of willis -

-frontal lobe dysfunction contralateral sensory loss in foot & leg paresis of arm & foot, relative sparing of thigh & face

-depends on whether its dominant of non dominant cortex contralateral hemiparesis contralateral hemisensory loss Aphasia/dysphasia apraxia

brain stem Cerebellum Occipital lobe

-Midbrain, Pons, Medulla -Midbrain Webers syndrome Pons medial &lateral inferior pontine syndromes Medulla Lateral medullary syndrome

homonymous hemianopia with macular sparing

DANISH dysdiadokinesis Ataxia Nystagus Intention tremor slurred speech Hypotonia

brain ischaemia and infarction Haemorrhages Vascular malformations and developmental abnormalities

-global hypoxia-ischaemic damage Focal infarcts- due to local vascular obstruction • generalised reduction in blood flow, global hypoxic ischaemic encephalopathy • systolic 50 -Mild: preferential loss of selectively vulnerable neurones Moderate: selective neuronal necrosis, glial and endothelial cells preserved Complete: pannecrosis -prolonged interruption of blood flow leading to irreversible ischeamic injury

• neurones (glial resistant) • resp obstruction, lung and heart disease, CO poisoning, cardiac arrest etc. • junctions or arterial territories and the first to be deprives of blood supply in hypotension e. g. superior cerebral convexities, posterior aspects of the cerebellar hemispheres

-Sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours -TIA evolving strokes complete strokes -Infarction: Thrombotic or Embolic Haemorrhagic: intracerebral subarachnoid Bleeding into infarct

-local interruption of cerebral, blood flow due to thrombosis or emboli -Atheroma Hypertension Serum lipids, obesity, diet Diabetes mellitus Heart disease Diseases of neck arteries Drugs Smoking -4-12 brain may appear normal 15-20 ischaemic neuronal changes develop, defined margin between normal brain 24-36 inflammatory reaction, extravasation of RBCs, activation and microglia 36-48 necrotic area visible, becomes swollen and softer than surrounding tissue day 3 macrophages infiltrate into area 1-2 weeks liquefaction of tissue and gloisis months cavitation and completion of glial scar

-spontaneous (rupture of saccular aneurysm, generally on internal carotid) or traumatic -bleeding into subarachnoid space intracerebral hematomas adjacent to aneurysms infarct of brain parenchyma due to arterial spasm -acute onset, no precipitating factors severe headache vomiting LOC